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. 2008 Jul 10;118(8):2733–2746. doi: 10.1172/JCI32381

Figure 9. Ang II–induced LR11/uPAR pathway in SMCs.

Figure 9

(A) uPAR expression in Lr11–/– SMCs. Membrane extracts of Lr11+/+ SMCs or Lr11–/– SMCs were incubated with or without Ang II (1 μM) in the presence or absence of sLR11 (1 μg/μl) and subjected to immunoblot analysis using anti-uPAR (~50 kDa) antibody. Blot shown is representative of 3 independent experiments. Data are presented as mean ± SD (n = 3). *P < 0.05. (B) Effect of blocking the LR11/uPAR pathway on the Ang II–dependent increase of Rac1 activation in rabbit SMCs. Cell lysates (60 μg protein) were incubated in the presence or absence of Ang II (1 μM) with or without valsartan (10 nM), anti-LR11 antibody, or anti-uPAR antibody, immunoprecipitated with PAK-1 PBD Protein GST beads, and subjected to immunoblot analysis using anti-Rac1 (~21 kDa) antibody. Blot shown is representative of 3 independent experiments. Data are presented as mean ± SD (n = 3). (C) Effect of ARB on the Ang II–dependent increase of Rac1 activation in Lr11–/– SMCs. Cell lysate (60 μg protein) of Lr11+/+ or Lr11–/– SMCs was incubated in the presence or absence of Ang II (1 μM) with or without candesartan (10 nM) or sLR11 (1 μg/μl), immunoprecipitated with PAK-1 PBD Protein GST beads, and subjected to immunoblot analysis using anti-Rac1 (~21 kDa) antibody. Blot shown is representative of 3 independent experiments. Data are presented as mean ± SD (n = 3).